What Is Selank? The Tuftsin-Derived Heptapeptide in GABAergic and Cytokine Research

Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, built by extending the natural tetrapeptide tuftsin (Thr-Lys-Pro-Arg) with a Pro-Gly-Pro tail. Tuftsin itself is a fragment generated from the heavy chain of immunoglobulin G, first described for its activity on phagocytic cells, but it is cleaved apart quickly by peptidases once it is in circulation. The Pro-Gly-Pro extension that defines Selank was added by researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences specifically to slow that breakdown and to produce a molecule with a distinct research profile from tuftsin itself. The published literature on Selank spans plasma enzyme assays, cultured neuroblastoma cells and rodent models, and covers several distinct lines of inquiry: effects on genes involved in GABAergic signaling, effects on cytokine and chemokine gene expression, inhibition of enkephalin-degrading enzyme activity, and changes in brain-derived neurotrophic factor (BDNF) expression. Separately from the research literature, Selank is registered as a pharmaceutical product in Russia, a regulatory fact noted here for background only and distinct from the laboratory research use of the compound described in this article.

What is tuftsin, and why extend it with Pro-Gly-Pro?

Tuftsin is a tetrapeptide corresponding to a short stretch of the heavy chain of immunoglobulin G, released from the parent antibody by proteolytic cleavage. Early characterization work described its activity on phagocytic cells and noted that, as a free tetrapeptide, it is a substrate for peptidases and is cleared from plasma within a short window, limiting its usefulness as a stable research tool (Siebert et al., 2017). Selank was designed by appending a Pro-Gly-Pro tripeptide to the C-terminus of tuftsin. This proline-rich extension is reported to reduce the rate at which the molecule is degraded by plasma peptidases relative to tuftsin itself, giving researchers a longer window to observe downstream effects in cell and animal preparations (Vyunova et al., 2018). This stability difference, more than any single shared activity, is why Selank is treated in the literature as a distinct research compound rather than a longer-lasting version of tuftsin.

What have gene-expression studies examined in the GABAergic system?

A Russian Academy of Sciences research group has used quantitative gene-expression methods to ask whether Selank administration changes transcription of genes involved in GABAergic neurotransmission. One study administered Selank to rats and measured expression of a panel of GABAergic-signaling genes in brain tissue, reporting shifts in several transcripts relative to untreated animals (Volkova et al., 2016). A follow-up study moved into cell culture, exposing IMR-32 human neuroblastoma cells to Selank, GABA itself, and olanzapine as comparators, and again measured the same gene panel, reporting that Selank produced expression changes that overlapped partially with those produced by GABA exposure in the same cell line (Filatova et al., 2017). Together, these two papers are the primary basis for describing Selank as a compound studied for GABAergic gene-expression effects in both whole-animal and cell culture systems.

What has research measured for cytokine and chemokine gene expression?

A separate set of experiments from the same program examined whether Selank and shorter fragments of its sequence change expression of genes encoding cytokines, chemokines and their receptors. Using quantitative mRNA methods, this work reported changes in a gene panel that included interleukin-6 alongside other cytokine and chemokine transcripts, comparing animals given Selank or its fragments with untreated controls (Kolomin et al., 2011). This line of inquiry sits alongside the tuftsin literature generally, since tuftsin and its analogs have long been studied for activity on immune cell populations, extending that interest to the transcript level rather than relying solely on earlier functional immune-cell assays.

What has research examined regarding enkephalin-degrading enzymes?

One proposed mechanism for Selank's effects in rodent behavioral models involves its action on enzymes that break down enkephalins, a class of endogenous opioid peptides. Using plasma samples and an enzyme activity assay, one study reported that Selank inhibited enkephalin-degrading enzyme activity, and proposed that this inhibition, by slowing endogenous enkephalin breakdown, could be one mechanism contributing to the behavioral effects observed in the same program's rodent studies (Zozulya et al., 2001). This finding is frequently cited as a candidate mechanism in later Selank papers, though it is one proposed pathway among several rather than a confirmed explanation for every effect reported in the broader literature.

What has research measured for BDNF expression?

Brain-derived neurotrophic factor is a protein involved in neuronal signaling and plasticity, and several short peptides studied in the Russian peptide research tradition have been examined for effects on its expression. One study administered Selank intranasally to rats and measured BDNF expression in hippocampal tissue, reporting a change in BDNF levels relative to untreated animals in this specific experimental model (Inozemtseva et al., 2008). This finding placed Selank alongside other short regulatory peptides studied for neurotrophic-factor effects in rodent brain tissue, a theme that recurs across several compounds from this same research lineage.

How does Selank relate to other research peptides?

Selank is most often discussed alongside Semax, another short synthetic peptide developed by related Russian research groups and studied for a partially overlapping set of effects; a direct comparison of the two sequences and their respective research literatures is covered separately in Selank vs Semax rather than repeated here. Selank's relationship to its parent tetrapeptide also places it within a broader category of short peptides derived from fragments of larger natural proteins, a design logic shared by the alpha-MSH-derived tripeptide covered in what is KPV. Selank is sometimes grouped informally with other short Russian-developed research peptides even though its tuftsin lineage and GABAergic and cytokine research focus differ mechanistically from the thymic- and pineal-tissue-derived compounds discussed in bioregulator peptides explained; researchers comparing across this wider category generally regard shared national research origin as a historical note, not evidence of a shared mechanism.

Handling notes

Selank is supplied as a lyophilized powder for research use. As with other short peptides, it should be stored according to the certificate of analysis and reconstituted using standard bench technique and concentration math appropriate to the planned assay, not as guidance for use in any subject. Confirm identity and purity from the lot-specific certificate of analysis before use in any laboratory procedure. A compound monograph covering Selank's background and research applications is available at our Selank learn page, and lot-specific specifications for research-grade Selank are posted on our Selank product page.

Frequently asked questions

Is Selank the same molecule as tuftsin?

No. Selank is a synthetic heptapeptide built by extending the natural tetrapeptide tuftsin with a Pro-Gly-Pro tail. The two molecules share the same first four amino acids but differ in length and, according to the published literature, in how quickly they are broken down by plasma enzymes.

What model systems have been used to study Selank?

Published studies have used rat brain and plasma samples, mouse behavioral assays, and IMR-32 human neuroblastoma cell culture, alongside enzyme activity assays conducted on plasma samples outside a living organism.

What outcome measures do these studies report?

Reported measures include expression levels of genes involved in GABAergic signaling, mRNA levels for cytokines and chemokines including interleukin-6, activity of enkephalin-degrading enzymes in plasma, and BDNF expression in rat hippocampal tissue.

Has Selank been studied in humans?

The studies summarized in this article are cell culture and rodent studies. This article describes laboratory research models, not clinical evidence, and nothing here describes a protocol for use in any subject.

Is Selank an approved medical product?

Selank is registered as a pharmaceutical product in Russia. This regulatory status is noted here as background information and is separate from, and does not apply to, the research use of the compound described in this article.

How is Selank supplied for laboratory use?

As a lyophilized powder intended for research use only, sold by lot with an accompanying certificate of analysis.

References

1. Siebert A, Gensicka-Kowalewska M, Cholewinski G, Dzierzbicka K. Tuftsin - Properties and Analogs. Curr Med Chem. 2017;24(34):3711-3727. PubMed 28745220.
2. Vyunova TV, Andreeva LA, Shevchenko KV, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914-923. PubMed 30255741.
3. Zozulya AA, Kost NV, Sokolov OY, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med. 2001;131(4):315-317. PubMed 11550013.
4. Volkova A, Shadrina M, Kolomin T, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016;7:31. PubMed 26924987.
5. Filatova E, Kasian A, Kolomin T, et al. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. Front Pharmacol. 2017;8:89. PubMed 28293190.
6. Kolomin TA, Shadrina MI, Slominsky PA, et al. Changes in expression of the genes for chemokines, cytokines, and their receptors in response to selank and its fragments. Genetika. 2011;47(5):711-714. PubMed 21786679.
7. Inozemtseva LS, Karpenko EA, Dolotov OV, et al. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008;421:241-243. PubMed 18841804.

Research use only. Homegrown Peptides products are for laboratory research and are not for human or animal use. Nothing in this article is medical advice.